Parental care and support in a safe environment are particularly important for mental health in social mammals, including humans and prairie voles. Studies of rodents and of lactating women suggest that oxytocin has the important capacity to modulate the behavioral and autonomic distress that typically follows separation from a mother, child, or partner, reducing defensive behaviors and thereby supporting growth and health (Carter, 1998).

During early life in particular, trauma or neglect may produce behaviors and emotional states in humans that are socially pathological. Because the processes involved in creating social behaviors and social emotions are delicately balanced, these be may be triggered in inappropriate contexts, leading to aggression toward friends or family.

Alternatively, bonds may be formed with prospective partners who fail to provide social support or protection.

Sex Differences In The Consequences Of Early Life Experiences

Males seem to be especially vulnerable to the negative effects of early experiences, possibly helping to explain the increased sensitivity of males to various developmental disorders. The implications of sex differences in the nervous system and in the response to stressful experiences for social behavior are only slowly becoming apparent (Carter et al., 2009).

Both males and females produce vasopressin and oxytocin and are capable of responding to both hormones. However, in brain regions that are involved in defensive aggression, such as the extended amygdala and lateral septum, the production of vasopressin is androgen-dependent.

Thus, in the face of a threat, males may be experiencing higher central levels of vasopressin.

Oxytocin and vasopressin pathways, including the peptides and their receptors, are regulated by coordinated genetic, hormonal, and epigenetic factors that influence the adaptive and behavioral functions of these peptides across the animal’s life span. As a result, the endocrine and behavioral consequences of a stress or challenge may be different for males and females (DeVries, DeVries, Taymans, & Carter, 1996).

For example, when unpaired prairie voles were exposed to an intense but brief stressor, such as a few minutes of swimming, or injection of the adrenal hormone corticosterone, the males (but not females) quickly formed new pair bonds. These and other experiments suggest that males and females have different coping strategies, and possibly may experience both stressful experiences, and even love, in ways that are gender-specific.

In the context of nature and evolution, sex differences in the nervous system are important. However, sex differences in brain and behavior also may help to explain gender differences in the vulnerability to mental and physical disorders (Taylor, et al., 2000). Better understanding these differences will provide clues to the physiology of human mental health in both sexes.

Loving Relationships In Early Life Can Have Epigenetic Consequences

Love is “epigenetic.” That is, positive experiences in early life can act upon and alter the expression of specific genes.

These changes in gene expression may have behavioral consequences through simple biochemical changes, such as adding a methyl group to a particular site within the genome (Zhang & Meaney, 2010). It is possible that these changes in the genome may even be passed to the next generation.

Social behaviors, emotional attachment to others, and long-lasting reciprocal relationships also are both plastic and adaptive, and so is the biology upon which they are based. For example, infants of traumatized or highly stressed parents might be chronically exposed to vasopressin, either through their own increased production of the neuropeptide, or through higher levels of vasopressin in maternal milk. Such increased exposure could sensitize the infant to defensive behaviors or create a lifelong tendency to overreact to threat.

Based on research in rats, it seems that in response to adverse early experiences of chronic isolation, the genes for vasopressin receptors can become upregulated (Zhang et al., 2012), leading to an increased sensitivity to acute stressors or anxiety that may persist throughout life.

Epigenetic programming triggered by early life experiences is adaptive in allowing neuroendocrine systems to project and plan for future behavioral demands. But epigenetic changes that are long-lasting also can create atypical social or emotional behaviors (Zhang & Meaney, 2010) that may be especially likely to surface in later life, and in the face of social or emotional challenges.

Exposure to exogenous hormones in early life also may be epigenetic. For example, prairie voles treated postnatally with vasopressin (especially males) were later more aggressive, whereas those exposed to a vasopressin antagonist showed less aggression in adulthood.

Conversely, in voles the exposure of infants to slightly increased levels of oxytocin during development increased the tendency to show a pair bond. However, these studies also showed that a single exposure to a higher level of oxytocin in early life could disrupt the later capacity to pair bond (Carter et al., 2009).

There is little doubt that either early social experiences or the effects of developmental exposure to these neuropeptides holds the potential to have long-lasting effects on behavior. Both parental care and exposure to oxytocin in early life can permanently modify hormonal systems, altering the capacity to form relationships and influence the expression of love across the life span.

Our preliminary findings in voles further suggest that early life experiences affect the methylation of the oxytocin receptor gene and its expression (Connelly, Kenkel, Erickson, & Carter, 2011). Thus, we can plausibly argue that love is epigenetic.

Authors: Sue Carter and Stephen Porges, University of North Carolina, Northeastern University - Boston. Reublished via Creative Commons.

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